Endothelial damage and dysfunction have been evidenced by increased levels of soluble adhesion molecules (e.g., sICAM-1, sVCAM-1 and sE-Selectin) and thrombomodulin (sTM), and reduced levels of nitric oxide (NO) in the plasma of patients with malaria [1], [2], [7]–[12]. The gene discussed is THBD; the disease is malaria.